Certain analogues of somatostatin (SRIF), like somatostatin itself, inhibit gastric acid secretion. For example, U.S. Pat. No., 4,061,626 discloses the activity of somatostatin, D-Lys.sup.4 -SRIF and D-Ala.sup.2, D-Lys.sup.4 -SRIF as gastric acid secretion inhibitors as well as inhibitors of growth hormone, glucagon and insulin secretion. Similarly U.S. Pat. No. 4,062,816 indicates that D-Ala.sup.5 -SRIF inhibits both gastric acid and growth hormone secretion. Inhibition of gastric acid secretion is, however, not a common attribute of all somatostatin analogues. For example, Lippmann et al., Pharmac. Res. Comm., 8 445 (1976) reports that D-Lys.sup.6 -SRIF had no appreciable effect on gastric acid secretion at a dose as high as 2 .mu.m/kg, s.c. Somatostatin has also been shown to reduce gastrointestinal bleeding. Horm. Metab. Res. 7 508 (1975).
It is known, as reported by Dollinger et al., Horm. Metab. Res. 8 74-78 (1976) that somatostatin reduces bicarbonate concentration slightly but significantly in duodenal aspirate of secretin treated patients and decisively reduces pancreatic enzyme secretion stimulated by pure cholecystokinin-pancreozymin (amylase, chymotrypsin and trypsin). At the same time, insulin secretion was significantly reduced.
The gastro-intestinal hormone gastrin is the most potent stimulant of gastric acid secretion known (1,500 times more potent than histamine on a molar basis). Gastrin is also a powerful stimulant of pancreatic enzyme secretion, being similar to cholecystokinin-pancreozymin in this regard. Zollinger-Ellison syndrome results from the release of large amounts of gastrin from tumors found primarily in the pancreas (these tumors are termed "gastrinomas").